Reduced Blood Viscosity Plays Minor Role in Regional Blood Flow Increases During Acute Normovolemic Hemodilution

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I read with interest the article by Barile et al,1 which describes a systematic review and meta-analysis of randomized trials demonstrating that acute normovolemic hemodilution (ANH) reduces allogenic red blood cell transfusion in cardiac surgery. The authors write that a beneficial effect of ANH is “improved perfusion during CPB through a decrease of blood viscosity resulting in an increased tissue O2 delivery above the critical anaerobic threshold,” but provide no data or cite literature to support this statement. Indeed, this characterization of the change in tissue perfusion during ANH is at variance with the well-described effects of ANH on regional blood flow and regional O2 delivery (the product of regional blood flow and arterial oxygen content).2 It has been demonstrated that ANH is accompanied by heterogeneous changes in regional blood flow reflecting the engagement of multiple vascular control mechanisms with varying regional influence. A significant role for reduced blood viscosity is not apparent. Blood flow increases in the heart, brain, and spinal cord are sufficient to maintain regional O2 delivery until hematocrit is reduced to below 10%.2,3 Markedly diminished hyperemic responses in these tissues during ANH3,4 provide evidence that their increases in blood flow during ANH are primarily, if not entirely, the result of vasodilation in response to decreased CaO2 rather than of reduced blood viscosity as suggested by Barile et al.1 This distinction is important because a dependence on vasodilation implies that a patient with a hemodynamically significant coronary or cerebral artery stenosis, in whom vascular reserve is compromised, would be at increased risk of regional tissue hypoxia during ANH. In such circumstances, ANH may be deemed unsafe and inappropriate or, in the least, require additional precautions. Blood flow in the peripheral organs, such as the kidney, gastrointestinal tract, and skeletal muscle, either increases modestly or remains constant during ANH, resulting in decreases in regional O2 delivery at relatively high hematocrit levels.2 The limited blood flow responses during ANH in these organs are consistent with a countervailing vasoconstrictor mechanism, perhaps an arterial chemoreceptor/sympathetic nerve reflex pathway, offsetting the effect of reduced blood viscosity.2 Notably renal blood flow remains constant during ANH, and thus regional O2 delivery decreases in parallel with hematocrit.2 Because a diffusive shunt for O2 exists in the kidney (owing to the close juxtaposition of the interlobar arteries and veins), an increase in renal O2 extraction cannot compensate for the decrease in regional O2 delivery during ANH, and both renal O2 uptake and tissue PO2 decline.2 These findings suggest that the kidney may be at particular risk of hypoxic damage during ANH.
A knowledge and understanding of the mechanisms underlying the changes in regional blood flow during ANH are necessary for its safe use as a method of blood conservation. There is no evidence that O2 delivery to any organ is maintained by the attendant reduction in blood viscosity. It is misleading to suggest that this occurs and to promote it as a benefit of ANH.
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